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Biomedical subjects

M M Scheinman

Publications and source records attributed to M M Scheinman.

At least 163 records · Page 9Linked to original sources
PubMed1988

Usefulness of sotalol for drug-refractory malignant ventricular arrhythmias.

Fifty patients with recurrent sustained symptomatic ventricular tachycardia (43 patients) or ventricular fibrillation (7 patients) resistant to a mean of 2.8 + 1.4 antiarrhythmic drugs were treated with sotalol, a beta-adrenergic receptor antagonist, and 45 underwent invasive electrophysiologic testing before and after sotalol therapy. The arrhythmia became noninducible in 10, was slower and hemodynamically well tolerated in 12 and was poorly tolerated in 23. Four patients were empirically treated with long-term administration of oral sotalol as were 21 patients who either had noninducible arrhythmia (10 patients) or had hemodynamically stable ventricular tachycardia (11 patients). In these 25 patients treated with long-term administration of sotalol, there was no recurrence of ventricular tachycardia in the group with noninducible arrhythmia, whereas 37% of patients with inducible ventricular tachycardia had new ventricular tachycardia or sudden death. Programmed ventricular stimulation with up to three extrastimuli proved to be an excellent predictor of drug efficacy and a good predictor of inefficacy. A positive prior response to amiodarone was not a reliable indicator of a positive response to sotalol. Side effects included those attributed to both beta-adrenergic blockade as well as proarrhythmic effects. The latter were observed in two of four patients with a QT interval greater than 600 ms. Sotalol was found to be effective therapy for a subset of patients with ventricular tachycardia unresponsive to type IA drugs.

Adult↗
PubMed1988

Electrocerebral accompaniments of syncope associated with malignant ventricular arrhythmias.

STUDY OBJECTIVE: To examine the electrocerebral and clinical accompaniments of syncope associated with malignant ventricular cardiac arrhythmias. DESIGN: Survey of clinical and electroencephalographic changes during induced cardiac dysrhythmia. SETTING: Clinical electrophysiology laboratory of a university medical center. PATIENTS: Fourteen patients with automatic cardioverter defibrillators due to previous cardiac arrest or life-threatening cardiac arrhythmia. INTERVENTION: Deliberate induction of cardiac dysrhythmia for routine, postoperative testing of the automatic implantable cardioverter defibrillator. Continuous electrocardiographic, electroencephalographic, and video recording. MEASUREMENTS AND MAIN RESULTS: Twenty-two episodes of ventricular tachycardia or fibrillation, lasting 15 to 126 seconds, were induced with definite loss of consciousness in 15 instances and probable loss in 2. In 10 episodes, there were motor accompaniments to the unconsciousness characterized by tonic activity or irregular muscle twitching. On regaining consciousness, patients were usually obtunded or confused for up to 30 seconds, depending on duration of induced cardiac dysrhythmia and unconsciousness. Electroencephalographic changes were variable. Background slowing was usually followed by relative loss of electrocerebral activity. In 2 patients, attenuation of background electrocerebral activity followed little or no change in background rhythms. In 5 episodes, electroencephalograms showed no change before loss of consciousness, but slowed thereafter in 4. CONCLUSIONS: Conspicuous motor activity may accompany syncope due to malignant ventricular arrhythmia and complicate the clinical distinction of syncope from seizures. Post-syncopal confusion generally lasts for less than 30 seconds. The electroencephalographic accompaniments of acute cerebral anoxia leading to syncope, and of the motor accompaniments of syncope, are more variable than previously appreciated, but electrographic seizure activity does not occur.

Adult↗
PubMed1987

Nonpharmacologic treatment of life-threatening cardiac arrhythmias.

Numerous nonpharmacologic modalities have been introduced for the management of patients with life-threatening arrhythmias. These include cardiac pacing, insertion of an automatic internal cardiac defibrillator (AICD), cardiac electrosurgery, and catheter ablative techniques. Each modality is effective; AICD shows particular promise because it has demonstrated remarkable efficacy in decreasing the incidence of sudden cardiac death in patients with malignant ventricular arrhythmias. Each modality also has its limitations or contraindications. Nonpharmacologic antiarrhythmic therapy represents an important advance against the serious public health problem of sudden cardiac death.

Arrhythmias, Cardiac↗
PubMed1987

Electrophysiologic testing and follow-up of patients with aborted sudden death.

Clinical, electrophysiologic and follow-up data were analyzed for 108 patients with aborted sudden death. The mean follow-up interval was 2 years. All patients underwent baseline drug-free invasive electrophysiologic studies. Seventy-five patients (group I) had inducible ventricular arrhythmias (including nonsustained and sustained ventricular tachycardia and ventricular fibrillation) and 33 patients (group II) had no inducible arrhythmias. Noninducibility was not predictive of a favorable outcome, because the incidence of both sudden death and recurrent ventricular tachycardia was similar in the two groups. Treatment guided by electrophysiologic testing was used in 17 patients; in 13 (17%) in group I arrhythmias became noninducible, and in 4 (5%) sustained ventricular arrhythmias became nonsustained after administration of conventional drugs. There was a significantly higher incidence of sudden death and recurrent ventricular tachycardia in the 4 patients with inducible arrhythmias (n = 3, 75%) compared with the 13 patients whose arrhythmias were noninducible (n = 2, 15%) (p less than 0.05). For the group as a whole, 11% died suddenly and 15% had recurrence of ventricular tachycardia. Sixty-four patients were treated with amiodarone and, of these, four (6%) died suddenly during the follow-up period and nine (14%) had recurrent ventricular tachycardia. Ventricular arrhythmias could be induced in 69% of patients with aborted sudden death but inducibility could be suppressed in only 20% of them. The role of therapy guided by electrophysiologic testing could therefore not be fully assessed. The findings reveal a significant recurrence rate of symptomatic, potentially life-threatening ventricular arrhythmias in medically treated patients with aborted sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Coexistent Mahaim and Kent accessory connections: diagnostic and therapeutic implications.

Six patients with coexistent Mahaim and Kent accessory connections are described. Two had left nodoventricular Mahaim connections, the first reported cases demonstrating these findings. In neither were the left-sided Mahaim connections components of a tachycardia and their presence was incidental. In two of four with nodoventricular connections, associated atrioventricular (AV) node conduction and coexistent posteroseptal accessory pathways were found. One of these had the unusual finding of a right-sided Mahaim connection arising from a "fast" AV node pathway. In only one patient did the tachycardia incorporate the Mahaim connection. In this patient, anterograde conduction during tachycardia occurred over a right nodoventricular connection whereas retrograde conduction occurred through a concealed right free wall Kent connection. Two patients had fasciculoventricular connections that were associated with either septal (one patient) or left free wall (one patient) Kent connections. The latter also had evidence of enhanced AV node conduction. This report is unique in that it describes in detail two patients with left nodoventricular connections (Mahaim) inserting in or near the left posterior fascicle. Combined Kent and Mahaim connections, present in the six patients, appear to occur in approximately 5% of patients with the Wolff-Parkinson-White syndrome. Precise identification of bypass connections critical for reentrant circuits is essential for intelligent application of treatment options.

Adult↗
PubMed1987

Permanent cardiac pacing in patients with the long QT syndrome.

A permanent pacemaker was inserted in eight patients with the long QT syndrome. All had recurrent syncope or seizures, six had documented torsade de pointes and four had aborted sudden death. Among the eight patients, permanent pacing was instituted in three who were unsuccessfully treated with both a beta-adrenergic blocking agent and left cardiothoracic sympathectomy, and in two who proved refractory or intolerant to beta-blockers. Another three patients had pacemaker implantation and long-term beta-blocker therapy because of spontaneous atrioventricular (AV) block in one, aborted sudden death in one and patient preference in one. After pacing (70 to 85 beats/min), there was no significant change in the mean corrected QT interval, but the mean QT interval decreased significantly (534.4 +/- 51.4 to 425.6 +/- 18.9 ms, p less than 0.0001). Over a mean follow-up period of 35.1 +/- 18.9 months, all patients are alive and currently free of syncope. One patient without a history of stress-induced syncope had two syncopal episodes (believed to be due to hyperventilation) while under severe emotional stress, but has been symptom free for the past 5 years. One patient with an atrial demand (AAI) pacemaker developed dizziness due to documented episodes of AV block, but remains asymptomatic after conversion to atrial rate-responsive dual chamber (DDD) pacing. Either atrial or ventricular pacing combined with beta-blocker therapy appears to be effective treatment for a subset of patients with the long QT syndrome, by either preventing episodes of torsade de pointes or alleviating symptoms due to bradycardia from beta-blocker therapy.

Adolescent↗
PubMed1987

Effects of catheter-delivered electrical discharges near the tricuspid anulus in dogs.

The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice failed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (less than 1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimal involvement was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Catheter ablation of ventricular tachycardia with intracardiac shocks: results in 33 patients.

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 33 patients who had recurrent unimorphic VT refractory to 3.7 +/- 1.2 (mean +/- SD) antiarrhythmic drugs. Their mean age was 56 +/- 14 years. Twenty-two patients had coronary artery disease, six had other types of heart disease, and five had no structural heart disease. The mean left ventricular ejection fraction was 0.34 +/- 0.17. Thirty patients had only one documented morphologic type of spontaneous VT, whereas three patients had more than one. One to four shocks of 100 to 300 J each were delivered to the endocardial exit site of VT, as identified by endocardial activation mapping and pace-mapping. In each patient endocardial activation at the exit site of VT preceded the onset of the QRS complex (mean activation time -50 +/- 30 msec). Pace-mapping was possible in 26 patients, and in all but two patients the QRS complexes during VT and during pacing at the exit site of VT were very similar in at least 10 of 12 electrocardiographic leads. In 29 patients, shocks were delivered between an endocardial electrode (cathode) and a patch electrode on the chest wall (anode). Seven patients (including three who first received shocks using an external anode) whose VT originated in the septum received transseptal shocks between two electrodes positioned on either side of the septum. The procedure was successful in 15 patients (45%), who had no recurrence of VT either on no antiarrhythmic therapy or on the same regimen that was ineffective before ablation, over a follow-up period of 15.5 +/- 10 months (range 5 to 35). The ablation attempt was unsuccessful in 18 patients (55%). There were no significant differences in clinical and electrophysiologic variables between patients with and without a successful outcome. Seven nonfatal complications occurred in six patients: sustained nonclinical VT immediately after the shock, ventricular fibrillation on days 5 and 6 after ablation, neurologic deficits (n = 2), atrioventricular block (n = 2), and brachial artery thrombosis. In conclusion, catheter electrical ablation of VT has modest efficacy and is relatively safe in a selected group of patients who have predominantly one configuration of unimorphic VT.

Cardiac Catheterization↗
PubMed1987

Long-term results of amiodarone therapy.

In order to assess the long-term efficacy of amiodarone, we followed 187 survivors of cardiac arrest and 316 patients with nonsustained or sustained ventricular tachycardia and compared the results of amiodarone therapy with the results of conventional therapy. All patients treated with amiodarone had failed to respond to one or more conventional agents. For survivors of cardiac arrest, survival of patients treated with amiodarone was equal to survival of patients treated with conventional agents. For patients with ventricular tachycardia, two-year survival was 91% in the conventional therapy group and 68% in the amiodarone group but incidence of sudden death was similar, probably reflecting increased non-sudden death due to advanced age and left ventricular dysfunction in the amiodarone-treated group. Side effects led to the discontinuation of amiodarone in approximately 25% of patients over a mean follow-up of 28 months. In a subgroup of patients who had demonstrated a proarrhythmic effect to Class I antiarrhythmic agents, amiodarone proved safe and effective. Amiodarone was well tolerated and effective therapy for atrial fibrillation in 59% of patients who had failed to respond to conventional agents. Thus, amiodarone is a useful option for patients with arrhythmias unresponsive to standard antiarrhythmic agents.

Adult↗
PubMed1986

Procainamide-induced incessant supraventricular tachycardia in the Wolff-Parkinson-White syndrome.

A patient with the Wolff-Parkinson-White syndrome presented with incessant orthodromic atrioventricular tachycardia following initiation of procainamide therapy. This finding was repeatedly documented both clinically as well as during electrophysiologic testing. Escape atrial complexes, which occurred following junctional premature complexes, failed to initiate tachycardia in the control state but tachycardia was always reinitiated by an identical escape sequence after procainamide. In addition, the tachycardia persisted and was repeatedly spontaneously reinitiated for prolonged periods after procainamide. The pro-arrhythmic effects of procainamide may be explained on the basis of both its vagolytic action on the atrioventricular node as well as by prolongation of refractoriness in the accessory pathway. These observations add to the literature on pro-arrhythmic effects of commonly used antiarrhythmic drugs.

Electrophysiology↗